Geris Flashcards

1
Q

How sensitive and specific is CAM (Confusion Assessment Method)
What does it involve?

A

94% sensitive, 89% specific

Acute onset, Inattention + either impaired consciousness or disorganised thinking

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2
Q

How to differentiate between delirium and dementia?

A

Delirium: acute, fluctuating, not orientated, impaired attention
Dementia: insidious onset, progressive, attention normally intact

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3
Q

What does the timed up and go test assess?

A

Mobility, balance and falls risk
Normal < 10s
Increased risk of falls in community dwelling adults >13.5s

Assesses falls risk

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4
Q

82yo mane presents with difficulty walking due to OA in his right hip. When prescribing a single point stick as a walking aide for him, the most appropriate instruction regarding use of the cane is:

A

Hold the cane on left hand and advance SPS with right leg - hold SPS in the “good” hand and advance with SPS with the ‘bad” leg

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5
Q

CADASIL - cerebral autosomal dominant arteriopathy with subcortical infarcts and leukenoencephalopathy

A

lacunar infarct, family history of dementia, dementia at young age, white matter disease, notch 3 gene, chromosome 19

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6
Q

Signs of normal pressure hydrocephalus

A

Cognitive impairment
Urinary incontinence
Dyspraxic gait

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7
Q

In Lewy Body dementia, what develops first - the dementia or parksinsons?

A

Dementia occurs first and then parkinsons later

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8
Q

What can help diagnose lewy body dementia?

A

SPECT scan - sensitivity 90%, specificity 100%

Low dopamine transporter uptake in basal ganglia on SPECT

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9
Q

3 types of frontotemporal lobar degeneration

A
  • Frontotemporal dementia (Pick’s disease)
  • Progressive non fluent aphasia (chronic progressive aphasia, CPA)
  • Semantic dementia
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10
Q

Name 3 cholinesterase inhibitors use to treated Alzheimers

A

Donepezil
Rivastigamine
Galantamine

“Dona Riva dances at the nursing home gala:” Donepezil, rivastigmine, and galantamine.

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11
Q

Benefit of cholinesterase inhibitors in Alzheimers

A

Improve cognitive function and improvement in activities of daily living

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12
Q

Adverse effects of cholinesterase inhibitors

A
  • GIT symptoms: upset stomach, nausea, diarrhoea, anorexia, weight loss occurs in 20-30% of patients
    Toxicity dose related, often resolves with time and dose reduction
  • Bradycardia from cholinergic toxicity
  • Headaches
  • Sleep disturbances like insomnia, vivid dreams, nightmares(happens with donepezil)
  • Can worsen urge incontinence
  • rarely rhabdo and NMS
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13
Q

Contraindications of cholinesterase inhibitors

A

Bradycardia, sick sinus syndrome, heart block, risk of fall/syncope/fractures

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14
Q

Mechanism of action of memantine and SE

A

NMDA antagonist used for moderate to severe Alzheimers
SE: headaches, dizziness, confusion, hallucinations , seizures
Should not use anticholinergic substances, eg: tricyclic antidepressants

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15
Q

Pathology of AD

A
  • Neuritic plaques (amyloid beta) accumulating extracellularly
  • Neurofibrillary tangles (phosphorylated tau) accumulating intracellularly
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16
Q

What infarcts are normally seen in vascular dementia?

A

Lacunar infarcts

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17
Q

What might be see on the SPECT scan for LBD?

A

Decreased occipital perfusion/metabolism

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18
Q

Pathology of lewy body dementia

A

a-synuclein

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19
Q

What might be see on the SPECT scan for frontotemporal dementia

A

Metabolic disorders in frontal and temporal lobes

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20
Q

What is order of language impairment in AD

A

naming - comprehension - fluency

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21
Q

Gene involved in familial alzheimer’s disease and what chromsome it is located on

A

PSEN1 on chromosome 14

22
Q

What chromosome is amyloid precursor protein located on?

A

chromosome 21

23
Q

Which allele has the strongest association with Alzheimer’s Disease

A

APOE4 alleles have the strongest associated with AD. Located on chromosome 19. one copy of E4 = 2x increased risk, 2 copies of E4 = 8x increased risk

24
Q

Which dementia are associated with tau?

A

Corticobasal degeneratin
Alzheimer’s Disease
Progressive supranuclear palsy

T-CAP

25
Q

Which dementia is associated with a-synuclein

A

Lewy body dementia
Parkinsons disease
Multisystem atrophy

(PALM)

26
Q

What dementia is associated with TDP43

A

Motor neuron disease
Limbic predominant age (LATE)
Frontotemporal dementia - primary progressive aphasia

27
Q

Pathophysiology of AD

A

Defining features of AD

  • Extraneuronal amyloid-β (Aβ) plaques [gun]
  • Neurofibrillary tangles (hyperphosphorylated tau) [bullet] - the main cause of AD
Microglia-mediated inflammation
Neuronal loss (inflammatory, oxidative)
28
Q

How are amyloid B plaques produced in alzheimer’s disease

A

Produced by proteolysis of transmembrane protein APP (amyloid precursor protein) by β and ɣ secretase enzy

29
Q

Disease burden of AD is dependent on what?

A

Severity of cognitive decline correlates more closely with NFT burden than with amount of amyloid deposition

30
Q

What areas of the brain are affected with neurofibrillary tangle pathology (tau)?

A

Entorhinal cortex (medial temporal lobe) > hippocampus >neocortex

31
Q

Quantity of B amyloid does not correspond to progression and severity of disease. T/F?

A

T
• Quantity does not correspond to progression and severity of disease
• Amyloid plaques commonly found in normal older adults
• Pharmacological clearance of amyloid-B has not resulted in improved cognition or ADLs
•Accumulating amyloid-B induces the spread of tau pathology (amyloid is the gun and tau is the bullet)
•Severity of cognitive decline correlates more closely with NFT burden than with amount of amyloid deposition

32
Q

What imaging modality should be used to diagnose vascular dementia?

A

Vascular dementia is the only dementia subtype where MRI is superior to CT, as cortical and subcortical ischaemic lesions are better demonstrated, and some vascular pathologies such as micro-bleeds may be otherwise missed.

33
Q

Difference between cerebral amyloid angiopathy and hypertensive bleeds.

A
  • Cerebral amyloid angiopathy characterised by haemorrhages in the cortex or subcortical white matter (lobar locations) with sparing of the basal ganglia and brainstem
  • In contrast, non-lobar haemorrhages or basal ganglia bleeds can be due to htn.
34
Q

What are the findings of lewy body dementia on spect?

A

decreased dopamine transporter uptake in basal ganglia on spect (sensitivity 90%, specificity 100%)

35
Q

What are features of lewy body dementia?

A
  • Dementia - impairments most in attention/concentration, executive function, visuospatial/constructional impairment instead of memory loss like in AD
  • Cognitive fluctuations
    Spontaneous and marked variations in cognition function, frequently accompanied by changes in alertness/arousal/consciousness
    ‘Staring spells’, ‘appears vague or blank’, ‘unresponsive but
    awake’, ‘confusion alternating with lucidity
  • Visual hallucinations - children and animals
  • Parkinsonism
  • REM sleep behaviour disorder
36
Q

What chromosome links familial FTD and amyotrophic lateral sclerosis (ALS)?

A

C9ORF72 (chromosome 9 opening reading frame 72)

37
Q

Indication of cholinesterase inhibitors

A

First-line treatment for Alzheimer dementia (particularly mild to moderate stages - MMSE 10-26) and vascular dementia.
Recommended for: Alzheimer disease, vascular dementia, lewy body dementia, parkinson disease dementia.
Not supported for:
Mild cognitive impairment
Frontotemporal dementia
Huntington disease
MS

38
Q

Indication of memantine

A

Particularly used in moderate to advanced cases (MMSE <10 or 10-14) of Alzheimer disease or vascular dementia

39
Q

Aducanumab

A

Aducanumab is a human, immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta.
For Alzheimer’s dementia

40
Q

Function of limbic cortex

A

Mood
Sleep + appetite
Attention + alertness

41
Q

Genetic factors associated with dementia

A
  • Down Syndrome (trisomy 21)
  • Amyloid precursor protein (APP): chromosome 21
  • Presenilin-1 (PSEN1): chromosome 14 (most common)
  • Presenilin 2 (PSEN2): chromosome 1
42
Q

Potentially modifiable RF for dementia

A

Early Life: Less education

Midlife: Hearing loss, traumatic brain injury, HTN, Alcohol, Obesity (in order)

Late Life: smoking, depression, social isolation, physical inactivity, air pollution, diabetes (in order)

43
Q

Variants of frontotemporal dementia and their features

A

(A) BEHAVIOURAL variant FTD

(B) LANGUAGE
(1) Semantic variant progressive primary progressive aphasia
- Issues with naming recognised objects, people and places
, slowly lose the knowledge of what the words mean
- Left anterior temporal atrophy
- Pathology: TDP 43

(2) Non-fluent/agrammatic variant primary progressive aphasia
- Gradual loss of ability to speak, read and write - can’t express themselves despite knowing the words, difficulty pronouncing words
- Left posterior fronto-insular atrophy
- Pathology: FTLD-T

(3) Logopenic variant primary progressive aphasia
- Left posterior temporal and inferior parietal atrophy

44
Q

Causes of rapidly progressive dementia

A
  • CJD
  • Neurodegenerative: Alzheimer’s, FTD, DLB
  • Vascular
  • Infectious: HIV, HSV-1, PML, TB, fungal, parasitic
  • Toxic: vitamins, alcohol, organ failure, heavy metals
  • Immunological / paraneoplastic
  • Malignant: CNS lymphoma
  • Iatrogenic due to hypotension, drugs, radiation
  • Seizures
45
Q
Mutations in the PSEN1 gene are the most common cause of familial AD. On which chromosome is PSEN1 gene found?
A. Chromosome 1
B. Chromosome 8
C. Chromosome 14
D. Chromosome 19
E. Chromosome 21
A

C. Chromosome 14

46
Q

The deposition of amyloid B plaques and neurofibillary tangles are 2 of the cellular hallmarks in the pathophysiology of AD. Which of the statements is not true?

A. Amyloid plaques are commonly found in normal older adults
B. The severity of cognitive decline correlates more closely with the amount of amyloid B then with neurofibrillary tangle burden
C. Amyloid plaques are produced by the proteolysis of transmembrane amyloid precursor protein by B and Y secretase enzymes
D. Tau promote stabilisation of intracellular microtubules in neurons
E. The entorhinal cortex is one of the earlies regions affected with neurofibillary tangle pathology

A

B. The severity of cognitive decline correlates more closely with the amount of amyloid B then with neurofibrillary tangle burden

47
Q
Which of the following modifiable midlife RF account for the greatest risk of developing dementia in later life?
A. TBI
B. HTN
C. Excess alcohol consumption 
D. Obesity
E. Hearing loss
A

E - hearing loss

48
Q

Which of the following would not be considered diagnostic for dementia with LB?
A. Cognitive fluctuations + severe neuroleptic sensitivity
B. Cognitive fluctuations + reduced uptake in BG on DAT scan
C. Parkinsonism + REM sleep behaviour disorder
D. Visual hallucinations + polysomnographic confirmation of REM sleep without atonia
E. Visual hallucinations + low uptake on MIBG scintigaphy

A

A. Cognitive fluctuations + severe neuroleptic sensitivity

49
Q

What medications leads to falls in the elderly?

A

Highest risk to lowest risk:

  • Antidepressants
  • Neuroleptics, antipsychotics
  • Benzos
  • Sedatives
  • Anti hypertensives
  • NSAID
  • Diuretics
  • B blockers
  • Narcotics
50
Q

What medications leads to falls in the elderly?

A

Highest risk to lowest risk:

  • Antidepressants
  • Neuroleptics, antipsychotics
  • Benzos
  • Sedatives
  • Anti hypertensives
  • NSAID
  • Diuretics
  • B blockers
  • Narcotics
51
Q

Subcortical vs cortical dementia

A

Subcortical dementia include diseases which predominantly affects the basal ganglia along with features of cognitive decline
Examples include progressive supranuclear palsy, Huntington’s chorea, corticobasal degeneration, multiple system atrophy
Clinically: slowness of mental processing, forgetfulness, impaired cognition, lack of initiative/apathy, depressive symptoms (anhedonia, negative thoughts, loss of self esteem), extrapyramidal features (tremors and abnormal movements)

Cortical dementia, eg: Alzheimer’s Dementia
Clinically: aphasia, agnosia, and apraxia